Week 12 / Pharmacology 2 Flashcards
Q: What are the 4 possible consequences of drug-receptor interactions?
Agonist
Antagonist
Allosteric modulator
Inverse Agonist
Q: What is an agonist drug?
A: An agonist drug mimics a natural, endogenous chemical messenger and produces the same effect.
Q: What is an antagonist drug?
A: An antagonist drug blocks the receptor and prevents the natural chemical messenger from binding, producing no effect.
Q: What is an allosteric modulator?
A: An allosteric modulator binds to a site near the binding site for the natural chemical messenger and influences its binding, producing either 1 or ½ the effect of the natural messenger.
Q: What is an inverse agonist drug?
A: An inverse agonist drug binds to the site normally occupied by a natural messenger and produces an opposite effect to the natural chemical messenger.
Q: What is the basic distinction between ‘Agonist’ and ‘Antagonist’ drugs?
A: Both agonist and antagonist drugs have affinity for their receptors
but only agonists have efficacy, meaning they can activate the receptor and cause a biological response
whereas antagonists have no efficacy and block the receptor without producing a response.
Q: What is efficacy in relation to drug-receptor interactions?
A: Efficacy is a measure of the ability of the drug-receptor complex to transduce the drug binding into a biological response. It expresses the ability of the drug to activate the receptor and cause a conformational change that leads to a biological effect.
Q: What is affinity in relation to drug-receptor interactions?
How is it expressed?
A: Affinity is a measure of the ease with which a drug binds to its receptor, or the probability that the drug will interact with a receptor to form a drug-receptor complex. It is expressed by the equilibrium dissociation constant (K), where affinity = 1/K.
Q: Do agonists have efficacy?
A: Yes, agonists have efficacy. They are able to activate the receptor and cause a biological response.
Q: Do antagonists have efficacy?
A: No, antagonists have no efficacy. They bind to receptors but do not activate them or cause a biological response.
Q: What does a high efficacy value (e) indicate?
A: A high efficacy value (e) indicates that the drug is highly effective at activating the receptor and producing a significant biological response.
Q: What is an agonist drug?
A: An agonist is a drug that binds to its receptor, activates the receptor, and elicits a biological response.
Q: What are the two types of agonists?
A: The two types of agonists are:
Full agonist
Partial agonist
Q: What is a full agonist?
A: A full agonist is a drug that binds to its receptor and produces the maximum possible biological response that the receptor can elicit.
Q: What is a partial agonist?
A: A partial agonist is a drug that binds to its receptor but produces a less than maximum biological response, even when all receptors are occupied.
Does the full agonist have high efficacy ?
A: A full agonist binds to its receptor, activates the receptor, and is capable of eliciting the maximum possible response. It has high efficacy.
Example: dobutamine, salbutamol.
What type of efficacy does partial agonist have?
What happens when a full agonist and partial agonist are both present?
A: A partial agonist binds to its receptor and activates it but can only elicit less than the maximum possible response. It has intermediate efficacy
reduces the response of a full agonist when both are present.
Example: buprenorphine, oxymetazoline.
Q: What is an antagonist drug?
A: An antagonist drug binds to its receptor but fails to activate it, resulting in no biological response. It has an efficacy (e) of 0.
Example: atenolol, chlorphenamine, naloxone.
Q: How does an antagonist drug produce its biological effect?
A: An antagonist produces its biological effect by competing with the agonist drug (or natural chemical messenger) for binding to the receptor, preventing the agonist from binding and eliciting a response.
Q: What is the ‘spare receptor’ or ‘receptor reserve’ concept?
A: The spare receptor or receptor reserve concept refers to the phenomenon where full agonists can elicit a maximum response without occupying all the available receptors.
This allows for economy of hormone or neurotransmitter secretion and enables low-affinity drugs to still produce the maximum possible response.
Q: How does the ‘spare receptor’ concept differ from the receptor occupancy theory?
A: The ‘receptor occupancy theory suggests that a drug’s biological effect is proportional to the fraction of receptors occupied, whereas the ‘spare receptor’ concept indicates that full agonists can produce a maximum response even if not all receptors are occupied.
Q: What is potency in the context of a graded dose-response curve?
When a lower dose is needed to achieve a response what does that indicate?
A: Potency is a measure of the amount of a drug needed to elicit a specified response. It is reflected in the location of the dose-response curve along the dose axis.
A lower dose needed to achieve a response indicates higher potency.
Q: How is potency experimentally and clinically expressed?
A: Experimentally, potency is expressed as ED50 (the dose required to produce 50% of the maximum response) or EC50 (the concentration at which 50% of the maximum effect is observed). Clinically, it is expressed as absolute or relative potency.
Q: Is potency a critical characteristic of a drug?
A: No, potency is not always a critical characteristic of a drug. For example, morphine and diamorphine (heroin) are both potent, but their effects differ, so potency does not necessarily determine therapeutic outcomes.
Q: What is maximal efficacy in the context of a graded dose-response curve?
A: Maximal efficacy refers to the maximum response or effect produced by a drug, reflected as a plateau in the log dose-response curve. It represents the drug’s ability to produce its therapeutic effect at its highest dose.
Q: Why is maximal efficacy important?
A: Maximal efficacy is the most important characteristic of a drug because it determines the maximum therapeutic effect that can be achieved. For example, paracetamol and morphine have different maximal efficacies due to their varying effectiveness in pain relief.
Q: Can maximal efficacy be limited in clinical practice?
A: Yes, maximal efficacy may be limited in clinical practice by the onset of adverse side effects. Even if a drug can theoretically produce a higher effect, its use may be restricted due to undesirable side effects.
Q: What does the slope of a graded dose-response curve represent?
A: The slope of the curve reflects the magnitude of change in response per unit change in dose. It shows how sensitive the response is to changes in drug concentration.
Q: How does the slope of the graded dose-response curve vary between drugs?
A: The slope can vary between drugs, with some drugs having a steeper slope, indicating a more rapid change in response to changes in dose, while others may have a flatter slope, showing a more gradual change in response.
Q: Why is the slope of the dose-response curve important in clinical practice?
A: The slope may be important because it can influence how quickly a drug achieves its effect in relation to dose changes, and may help clinicians determine the appropriate dose for achieving desired therapeutic effects with minimal side effects.
Q: What is biological variability in the context of drug response?
A: Biological variability refers to differences in drug response between individuals or even within the same individual, despite receiving the same dose of the drug.
Q: What are some sources of biological variability in drug response?
A: Sources of biological variability include:
Age
Gender
Genetic factors
Polypharmacy (use of multiple drugs)
Pathological state (e.g., diseases or conditions affecting drug metabolism)
Q: How does biological variability affect drug response in the same individual?
A: Even in the same individual, biological variability can lead to different responses to the same dose of a drug due to factors like changes in health, diet, or drug interactions.
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